|Regulation of adiposity by dietary calcium.|
|PMID: 10834935 Owner: NLM Status: MEDLINE|
|Recent data from this laboratory demonstrate that increasing adipocyte intracellular Ca(2+) results in a coordinated stimulation of lipogenesis and inhibition of lipolysis. We have also noted that increasing dietary calcium of obese patients for 1 year resulted in a 4.9 kg loss of body fat (P<0.01). Accordingly, we tested the possibility that calcitrophic hormones may act on adipocytes to increase Ca(2+) and lipid metabolism by measuring the effects of 1, 25-(OH)(2)-D in primary cultures of human adipocytes, and found significant, sustained increases in intracellular Ca(2+) and a corresponding marked inhibition of lipolysis (EC(50) approximately 50 pM; P<0.001), suggesting that dietary calcium could reduce adipocyte mass by suppressing 1,25-(OH)(2)-D. To test this hypothesis, we placed transgenic mice expressing the agouti gene specifically in adipocytes on a low (0.4%) Ca/high fat/high sucrose diet either unsupplemented or with 25 or 50% of the protein replaced by non-fat dry milk or supplemented to 1.2% Ca with CaCO(3) for 6 wk. Weight gain and fat pad mass were reduced by 26-39% by the three high calcium diets (P<0.001). The high calcium diets exerted a corresponding 51% inhibition of adipocyte fatty acid synthase expression and activity (P<0.002) and stimulation of lipolysis by 3. 4- to 5.2-fold (P<0.015). This concept of calcium modulation of adiposity was further evaluated epidemiologically in the NHANES III data set. After controlling for energy intake, relative risk of being in the highest quartile of body fat was set to 1.00 for the lowest quartile of Ca intake and was reduced to 0.75, 0.40, and 0.16 for the second, third, and fourth quartiles, respectively, of calcium intake for women (n=380;P<0.0009); a similar inverse relationship was also noted in men (n=7114; P<0.0006). Thus, increasing dietary calcium suppresses adipocyte intracellular Ca(2+) and thereby modulates energy metabolism and attenuates obesity risk.|
|M B Zemel; H Shi; B Greer; D Dirienzo; P C Zemel|
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|Type: Journal Article; Research Support, Non-U.S. Gov't|
|Title: FASEB journal : official publication of the Federation of American Societies for Experimental Biology Volume: 14 ISSN: 0892-6638 ISO Abbreviation: FASEB J. Publication Date: 2000 Jun|
|Created Date: 2000-07-12 Completed Date: 2000-07-12 Revised Date: 2012-02-15|
Medline Journal Info:
|Nlm Unique ID: 8804484 Medline TA: FASEB J Country: UNITED STATES|
|Languages: eng Pagination: 1132-8 Citation Subset: IM|
|Department of Nutrition, The University of Tennessee, Knoxville, Tennessee 37996-1900, USA. email@example.com|
|APA/MLA Format Download EndNote Download BibTex|
Agouti Signaling Protein
Blood Glucose / analysis
Body Temperature / drug effects
Calcium / metabolism*
Calcium, Dietary / administration & dosage, pharmacology*, therapeutic use
Energy Metabolism / drug effects
Fatty Acid Synthetase Complex / genetics, metabolism
Insulin / blood
Intercellular Signaling Peptides and Proteins*
Lipolysis / drug effects*
Obesity / blood, diet therapy, metabolism
Parathyroid Hormone / antagonists & inhibitors, pharmacology
Proteins / genetics, metabolism
Vitamin D / antagonists & inhibitors, pharmacology
Weight Gain / drug effects
|0/Agouti Signaling Protein; 0/Blood Glucose; 0/Calcium, Dietary; 0/Insulin; 0/Intercellular Signaling Peptides and Proteins; 0/Parathyroid Hormone; 0/Proteins; 1406-16-2/Vitamin D; 7440-70-2/Calcium; EC 6.-/Fatty Acid Synthetase Complex|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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